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Background: Biomarkers for the early prediction of the severity of acute pancreatitis (AP) are urgently needed for clinical management of the disease. Angiopoietin-2 (Ang-2), one of the autocrine peptides that reduce endothelial permeability, has been found to be associated with various diseases, including inflammatory disorders., Aims: This study aimed to determine whether serum Ang-2 could serve as a noninvasive biomarker for the early prediction of persistent organ failure (POF) in acute pancreatitis., Methods: A total of 120 AP patients were prospectively enrolled at Jinling Hospital. Serum samples were collected on admission. Clinical and laboratory data were recorded. Ang-2 levels were measured by enzyme-linked immunosorbent assay., Results: A total of 37 patients developed POF and were classified as having severe AP (SAP). Ang-2 was significantly higher on admission in patients who developed POF than in those who did not (p < 0.001 for all). Furthermore, receiver operating characteristic (ROC) curve analysis revealed that Ang-2 could distinguish patients who developed POF from mild AP (MAP, area under ROC curve [AUC] = 0.88, 95 % CI 0.78-0.94) and moderately severe AP patients (MSAP, AUC = 0.74, 95 % CI 0.63-0.83). In addition, multivariate logistic regression showed that increased Ang-2 was an independent predictor of developing POF between subgroups with MSAP and SAP (OR 7.2, 95 % CI 2.7-19.4) and among all AP patients (OR 12.1, 95 % CI 4.8-30.3)., Conclusions: Elevated serum Ang-2 levels on admission may be a promising biomarker for the prediction of POF in AP.

Objectives: Acute pancreatitis (AP) is a severe inflammatory disease with high mortality and morbidity rates. We have previously demonstrated that resistin may represent an early marker of inflammation in AP. It was also revealed that ghrelin may have anti-inflammatory potential. However, the role of adipohormones in AP-resistin and ghrelin as well as the proinflammatory cytokine interleukin (IL)-18-has not yet been fully elucidated., Methods: The study group comprised 32 patients with alcoholic AP and 30 controls matched for age, sex, and body mass index (BMI). In all cases AP was classified as grade C according to Balthazar's computed tomography (CT) score and as severe (3 points) according to Ranson's criteria. Serum levels of resistin, ghrelin, and IL-18 were measured on first, third, and fifth day of hospitalization by enzyme-linked immunosorbent assay (ELISA)., Results: On first day of hospitalization the mean serum resistin concentration in AP patients was significantly higher than in controls (P < 0.05) and further increased on third and fifth day of hospitalization (17.4 ± 4.23 ng/ml and 25.8 ± 8.14 ng/ml, respectively). On first day of hospitalization the mean serum IL-18 concentration in AP patients was significantly higher than in controls (P < 0.05), on third day its level further increased, and on fifth day it decreased to a level similar to that observed on admission. The serum ghrelin concentrations on first, third, and fifth day of hospitalization were comparable, and significantly higher than in controls (P < 0.01). Significant correlation between C-reactive protein (CRP) and resistin levels (r = 0.43; P < 0.05) and between CRP and IL-18 (r = 0.58; P <0.05) on day of admission was found., Conclusions: Serum concentration of IL-18 and resistin may contribute to inflammatory response and may be useful as an early marker of inflammation in AP. We also suspect that ghrelin affects the course of AP and plays an important role in inflammatory response.

Trypsin-like activity is released after stimulation of the exocrine pancreas. We investigated under basal conditions and after stimulation by a meal whether patients suffering from pancreatic disorders differ with respect to plasma trypsin-like activity (PTLA). In 45 subjects (healthy volunteers: n = 18, mild/moderate alcoholic chronic pancreatitis: n = 16, nonjaundice pancreatic cancer n = 7, and calcifying chronic pancreatitis: n = 4), basal and postprandial levels of PTLA were measured over a period of 2 hours. Basal plasma levels were similar in the first 3 groups. After stimulation, healthy volunteers and patients with pancreatic cancer showed significant decreases in trypsin-like activity; however, plasma levels did not decrease in patients with mild/moderate chronic pancreatitis (P < .001). Healthy individuals demonstrate a consistent decrease in postprandial trypsin-like plasma activity. This response is not altered in patients with pancreatic cancer, and it is not seen in patients with mild/moderate alcoholic chronic pancreatitis.

The exact immunological mechanisms underlying alcoholic chronic pancreatitis are unclear. To investigate the role of the tumor necrosis factor (TNF) receptor pathway the serum levels of TNF-alpha, soluble TNF receptors -p55/-p75, and CRP were determined by ELISA in 34 patients with late-stage alcoholic chronic pancreatitis and 28 controls. The disease activity (Balthazar scoring system) of acute pancreatitis on the background of late-stage chronic pancreatitis correlated with an increase of functionally active TNF receptor -p55/-p75 serum levels. Unstimulated peripheral blood mononuclear cells are one source of soluble TNF receptors and demonstrated a systemic leukocyte activation. The marked enhancement of soluble TNF receptors suggests that alcoholic chronic pancreatitis may be characterized by transient peaks of in situ TNF-alpha production preceding a long-lasting release of soluble TNF receptors. The data demonstrate immunological changes characteristic of acute pancreatitis in late-stage alcoholic chronic pancreatitis.

Interleukin 10 (IL-10) recently emerged as an antiinflammatory cytokine that inhibits the secretion of proinflammatory cytokines by monocytes and/or macrophages and the release of free oxygen radicals. It has been reported that treatment with IL-10 decreases the severity of experimental pancreatitis, mainly by inhibiting cellular necrosis. The aim of this study was to evaluate the behavior of serum IL-10 in patients with acute pancreatitis and to explore the possibility of a relationship between this cytokine and severity of the disease. Forty-five patients with acute pancreatitis were studied. Acute pancreatitis was of biliary origin in 30 patients, due to alcohol abuse in 10, due to pancreas divisum in 1, and of unknown origin in the remaining 4. According to the Balthazar criteria, 19 patients had scores of A, B, or C and 25 had scores of D or E. Twelve healthy subjects were also studied as controls. Serum IL-10 was determined in all subjects on admission, and in acute pancreatitis patients also daily for the following four days using a commercial kit. Healthy subjects had no detectable serum levels of IL-10. In acute pancreatitis patients, serum IL-10 levels were increased on the first day of the disease and then progressively decrease in the following days. On the first day of the acute pancreatitis, patients with the mild disease had serum levels of IL-10 significantly higher than those with severe disease, whereas in the following days, no statistically significant difference was observed between the two groups. The elevation of IL-10 on the first day of the illness is more marked in patients with mild acute pancreatitis than in those with the severe form of the disease. The finding of low values of serum IL-10 in severe acute pancreatitis suggests that there may be altered down-regulation of the immune system response in these patients.